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(Hypertension. 2009;53:112.)
© 2009 American Heart Association, Inc.

Editorial Commentaries

Mitochondrial Dysfunction and Mitochondrial-Produced Reactive Oxygen Species

New Targets for Neurogenic Hypertension?

From the Department of Cellular and Integrative Physiology (M.C.Z., I.H.Z.), University of Nebraska Medical Center, Omaha; and the Redox Biology Center (M.C.Z.), University of Nebraska, Lincoln.

Correspondence to Irving H. Zucker, University of Nebraska Medical Center, Department of Cellular and Integrative Physiology, 985850 Nebraska Medical Center, Omaha, NE 68198-5850. E-mail izucker@unmc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Over the past 10 to 15 years, a vast collection of studies have provided evidence indicating that reactive oxygen species (ROS), particularly superoxide (O₂^·–) and hydrogen peroxide (H₂O₂), contribute to the pathogenesis of cardiovascular diseases, such as heart failure and hypertension. Griendling et al¹ first demonstrated that NADPH oxidase present in the vasculature is a primary source of the elevated ROS levels. Since these initial studies, NADPH oxidase-derived ROS in the kidney,² heart,³ and brain⁴ have been linked to the development and progression of numerous cardiovascular-related diseases. More recently, however, mitochondria have also been identified as important sources of ROS in controlling cardiovascular function. Considering that mitochondria are the primary source of ROS in most cells during normal respiration because of the leaking of electrons from the electron transport chain (ETC), perhaps it should not be all that surprising that mitochondrial-produced ROS are involved in pathophysiological conditions of the cardiovascular system.

To date, most of the evidence linking mitochondrial dysfunction and mitochondrial-produced ROS to the pathogenesis of cardiovascular diseases comes from studies on the peripheral renin-angiotensin system.⁵ For example, using a model of cardiac ischemic reperfusion injury, Kimura et al⁶ reported that angiotensin II (Ang II)-induced preconditioning is mediated by mitochondrial-produced ROS. The authors further demonstrated that Ang II-induced NADPH oxidase-derived ROS lie upstream of mitochondrial-produced ROS, thus, implicating a ROS-induced ROS mechanism. Similarly, it was demonstrated recently that, in aortic endothelial cells, Ang II-induced NADPH oxidase activation leads to an increase in mitochondrial ROS production, as . . . [Full Text of this Article]

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